Urea and Na+ permeabilities in toad urinary bladder: one or two solute pathways?

Abstract

It has been reported that toad urinary bladder amiloride not only reversibly blocks Na+ transport, but it also reversibly inhibits urea permeability (Pu). This finding prompted some queries: 1) Does Na+ transport rates and/or the cytosolic Na+ pool regulate Pu? 2) Does amiloride inhibit two different solute pathways or one pathway through which both Na+ and urea permeate? The following results were obtained in toad bladder. 1) The absence of mucosal Na+ does not interfere with basal or ADH-induced Pu. 2) Amiloride inhibits Pu in the absence of apical Na+. 3) The concentration of amiloride that produces half-maximal inhibition (K1/2) of the ADH-induced Na+ transport is 7 X 10(-7)M with 110 mM mucosal Na+, 7 X 10(-8)M with 1 mM apical Na+, and 2 X 10(-6)M in the absence of mucosal Ca2+; K1/2 of ADH-stimulated Pu is 9 X 10(-5)M and is not altered by lowering the mucosal Na+ concentration to 1 mM or deleting apical Ca2+. 4) Mucosal La3+ (10(-3)M): i) reversibly increases Na+ transport by 75%, potentiating the natriferic effect of ADH by 51%; ii) does not affect basal Pu and irreversibly blunts the ADH-mediated increase in Pu by 72%; and iii) has no effect on basal or ADH-induced osmotic flow. Identical results were obtained with Tm3+. These results suggest that the inhibitory effect of amiloride on amide permeation is not mediated by its effect on Na+ transport. There are three separate operational pathways for water, Na+, and urea; amiloride reversibly blocks those through which Na+ and urea permeate.(ABSTRACT TRUNCATED AT 250 WORDS)